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Thrombotic Disorders Flashcards

1
Q

What is venous thromboembolism?

A

Venous thromboembolism is the process of blood clot formation in the veins.

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2
Q

What is the difference between provoked and unprovoked VTE?

A

Provoked VTE is associated with a clear precipitating cause from history or tests, while unprovoked VTE has no clear cause.

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3
Q

What is thrombophilia?

A

Thrombophilia refers to a condition where the blood in the body clots more easily than normal.

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4
Q

What are the causes of circulatory stasis, a component of Virchow’s triad?

A

Causes of circulatory stasis include bed rest, lower limb orthopedic surgery, major abdominal surgery, pregnancy, and long haul flights/long car journeys.

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5
Q

What are the causes of hypercoagulable states?

A

Causes of hypercoagulable states include smoking, oestrogens (oral contraceptives, HRT), active cancer, and inherited and acquired thrombophilias.

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6
Q

What are the causes of vascular injury, another component of Virchow’s triad?

A

Causes of vascular injury include limb trauma (including surgery), foreign bodies (e.g., IV cannulae, pacemaker wires), sepsis (bacteria, toxins), and previous DVT (deep vein thrombosis). May-Thurner Syndrome is also a cause of vascular injury.

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7
Q

What is the most common inherited thrombophilia?

A

The most common inherited thrombophilia is Factor V Leiden, which is caused by a mutation of the Factor V gene.

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8
Q

What is the second most common inherited thrombophilia?

A

The second most common inherited thrombophilia is prothrombin thrombophilia, caused by a Factor II gene mutation.

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9
Q

What are some other forms of inherited thrombophilias?

A

Other inherited forms of thrombophilia include protein C deficiency, protein S deficiency, hereditary anti-thrombin deficiency, and congenital dysfibrinogenemia.

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10
Q

When should testing for inherited thrombophilias be considered?

A

Testing for hereditary thrombophilia should be considered in individuals who have had unprovoked deep vein thrombosis (DVT) or pulmonary embolism (PE) and have a first-degree relative who also had DVT or PE, especially if there is a plan to stop anticoagulation treatment.

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11
Q

Should thrombophilia testing be routinely offered to first-degree relatives of people with a history of DVT or PE and thrombophilia?

A

No, routine thrombophilia testing should not be offered to first-degree relatives of people with a history of DVT or PE and thrombophilia.

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12
Q

Should testing for hereditary thrombophilia be offered to people who are already on anticoagulation treatment?

A

No, testing for hereditary thrombophilia should not be offered to people who are already on anticoagulation treatment.

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13
Q

Should thrombophilia testing be offered to people who have had provoked DVT or PE?

A

No, thrombophilia testing should not be offered to people who have had provoked DVT or PE.

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14
Q

What is the most common acquired thrombophilia?

A

The most common acquired thrombophilia is antiphospholipid syndrome, which is an autoimmune disorder where antibodies attack phospholipids.

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15
Q

What is the gender distribution of antiphospholipid syndrome?

A

Antiphospholipid syndrome is more commonly seen in females, with approximately 70% of cases occurring in women.

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16
Q

What is the association between antiphospholipid syndrome and Systemic Lupus Erythematosus (SLE)?

A

Approximately 10-15% of people with Systemic Lupus Erythematosus have antiphospholipid syndrome.

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17
Q

What are the increased risks of pregnancy complications in individuals with antiphospholipid syndrome?

A

Individuals with antiphospholipid syndrome have an increased risk of miscarriage, stillbirth, and pre-eclampsia.

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18
Q

What is the second most common acquired thrombophilia?

A

The second most common acquired thrombophilia is acquired dysfibrinogenemia, which can be caused by conditions such as severe liver disease, autoimmune disease (e.g., rheumatoid arthritis), plasma cell dyscrasias (e.g., myeloma), and certain cancers (e.g., cervical cancer).

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19
Q

What is the common clinical presentation of deep vein thrombosis (DVT)?

A

Clinically, DVT may present with unilateral calf swelling, heat, pain, redness, and hardness. However, it is important to note that there can be no signs or symptoms in some cases.

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20
Q

What is the most common site of deep vein thrombosis (DVT)?

A

The most common site of DVT is in the calf, particularly in the popliteal and tibial veins. DVT can also occur in the thigh, involving the femoral and iliac veins.

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21
Q

What are some differential diagnoses for deep vein thrombosis (DVT)?

A

Some differential diagnoses for DVT include Baker’s cyst, cellulitis, and muscular pain.

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22
Q

What are the risk factors associated with DVT?

A

Risk factors for DVT include a history of previous DVT, immobility, surgery, pregnancy, cancer, obesity, and certain medical conditions such as thrombophilias.

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23
Q

What is the D-dimer test used for in the investigation of DVT?

A

The D-dimer test is useful to rule out DVT if the clinical probability is low. It measures the level of D-dimer, a breakdown product of fibrin, which is elevated in venous thromboembolism.

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24
Q

What is the investigation of choice for DVT?

A

Doppler ultrasound is the investigation of choice for DVT. It provides real-time 2D images and uses color Doppler (Duplex) to show the direction and velocity of blood flow. Thrombosed veins appear non-compressible on ultrasound.

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25
Q

When is contrast venography rarely required in the investigation of DVT?

A

Contrast venography is rarely required but can be useful in extensive disease or when looking for anatomical malformations.

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26
Q

What is the significance of D-dimer in DVT diagnosis?

A

D-dimer is a breakdown product from fibrin, the fibrous mesh component of blood clots. It is only present when the coagulation system has been activated. An elevated D-dimer level is seen in venous thromboembolism. A negative D-dimer test can be used to rule out DVT or PE if the clinical probability is low. However, a positive D-dimer test is not diagnostic on its own.

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27
Q

Are there any limitations of the D-dimer test?

A

Yes, the D-dimer test is very sensitive but not very specific. Occasionally, it can be negative in cases of large or extensive DVTs or PEs. Therefore, it should not be used if there is a high clinical probability of DVT or PE.

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28
Q

What is the treatment approach for DVT limited to the calf?

A

For DVT limited to the calf, symptomatic treatment is provided. Repeat ultrasound is done in 7 days to ensure no progression of the clot.

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29
Q

How is ilio-femoral DVT treated?

A

Ilio-femoral DVT is treated with anticoagulation using Direct Oral Anticoagulants (DOACs) such as Rivaroxaban or Dabigatran. The duration of anticoagulation is 3-6 months for the first event and lifelong for the second event. Warfarin may be used in cases of renal dysfunction.

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30
Q

When should thrombophilia testing be considered in the treatment of DVT?

A

Thrombophilia testing should be considered if there is a first-degree relative with a history of venous thromboembolism (VTE).

31
Q

What are the clinical presentations of pulmonary embolism (PE)?

A

The clinical presentation of PE can vary depending on the size and location of the emboli. Microemboli are often asymptomatic. Small, peripheral emboli may present with pleuritic pain, breathlessness, and haemoptysis. Large, central emboli can cause chest pain, breathlessness, and hypoxia. Massive emboli can lead to syncope, shock, tachycardia, and even death.

32
Q

What are some diagnostic findings in pulmonary embolism (PE)?

A

In PE, oxygen saturations are typically low, and blood gas analysis shows a low PaO2. Electrocardiogram (ECG) may reveal sinus tachycardia (fast heart rate) and characteristic findings such as S1, QIII, TIII. An echocardiogram may show signs of right heart strain.

33
Q

What is CTPA, and when is it used in the diagnosis of PE?

A

CTPA stands for CT pulmonary angiogram, which is a CT scan used to visualize the pulmonary arteries and detect blood clots. CTPA carries a high radiation dose and is typically used if there is a reasonable likelihood of PE. However, it is important to consider alternative approaches in some groups of patients.

34
Q

What is the Wells score used for in the investigation of PE?

A

The Wells score is a scoring system used to assess the probability of PE. It helps guide the decision-making process regarding further investigations.

35
Q

How is a low probability of PE investigated?

A

In cases of low probability of PE, a D-dimer test is performed first. If the D-dimer test is positive, indicating a possible clot, a CTPA may be conducted to confirm the diagnosis.

36
Q

What is a ventilation-perfusion lung scan?

A

A ventilation-perfusion (V/Q) lung scan is a nuclear medicine test that involves inhaled and injected radioisotopes. It assesses the mismatch between lung ventilation and perfusion, helping to detect areas of the lung with abnormal blood flow. However, its use may be limited in the presence of underlying lung disease.

37
Q

When is a ventilation-perfusion lung scan used in the diagnosis of PE?

A

A ventilation-perfusion lung scan is used as an alternative to CTPA when CTPA is contraindicated. This includes situations such as severe contrast allergy, severe renal dysfunction, or a high risk from radiation exposure.

38
Q

What factors should be considered when choosing anticoagulation therapy for PE treatment?

A

When selecting anticoagulation therapy for PE treatment, it is important to consider co-morbidities, contraindications, and patient preferences. Assessing bleeding risk using a scoring system such as HASBLED can help guide decision-making.

39
Q

What are some special circumstances to consider in PE treatment?

A

Special circumstances in PE treatment include renal function, body weight extremes, cancer-associated thrombosis, and antiphospholipid syndrome (APLS).

40
Q

What is the initial treatment for large PE?

A

For large PE, initial treatment typically involves the administration of heparin, usually subcutaneous low molecular weight heparin (e.g., Enoxaparin).

41
Q

How long is anticoagulation therapy continued after a PE?

A

Following a first event of PE, anticoagulation therapy is usually continued for 3-6 months. In the case of a second event or persistent risk factors (e.g., thrombophilia), lifelong anticoagulation may be necessary.

42
Q

Can smaller PEs be treated with direct oral anticoagulants (DOACs) without initial heparin therapy?

A

Yes, smaller PEs can be treated directly with DOACs without the need for initial heparin therapy.

43
Q

What treatment options are available for massive PE?

A

Treatment for massive PE includes intravenous fluids, intravenous heparin infusion, and consideration of thrombolysis. Thrombolysis may be considered if the patient is in shock or shows signs of right heart strain. Other options include surgical embolectomy or catheter fragmentation.

44
Q

What are some measures for VTE prevention?

A

VTE prevention measures include prophylactic low-dose subcutaneous heparin, low-dose Rivaroxaban after major joint surgery, venous compression stockings, pneumatic compression stockings, early mobilization, and maintaining good hydration.

45
Q

What is the role of von Willebrand factor (vWF) in platelet adhesion?

A

vWF acts as a molecular bridge between platelets and exposed collagen, facilitating platelet adhesion.

46
Q

How do platelets become activated?

A

Platelets become activated through various interactions, including the binding of vWF to glycoprotein 1b-IX-V complexes, leading to platelet tethering and rolling along the endothelial surface.

47
Q

What is the function of glycoprotein 2b/3a (GP2b3a) on platelets?

A

GP2b3a on activated platelets binds to fibrinogen, facilitating platelet aggregation and clustering.

48
Q

What is the role of thromboxane A2 in platelet function?

A

Thromboxane A2, generated from arachidonic acid under the influence of cyclooxygenase, promotes platelet activation, aggregation, and adhesion by binding to thromboxane receptors on other platelets.

49
Q

What are the main uses of antiplatelet medications?

A

Antiplatelets are used to prevent or treat conditions involving excessive platelet activation, such as atherosclerosis, coronary artery disease, and stroke.

50
Q

What is the mechanism of action of antiplatelet drugs?

A

Antiplatelet drugs inhibit platelet function by targeting various pathways, such as blocking the activation of glycoprotein 2b/3a receptors or inhibiting the production of thromboxane A2.

51
Q

What are some common side effects of antiplatelet medications?

A

Common side effects of antiplatelets may include increased risk of bleeding, gastrointestinal disturbances, allergic reactions, and bruising.

52
Q

What are the common side effects of aspirin?

A

Peptic ulceration, rash, and high doses may cause hearing loss/tinnitus. In children given aspirin for viral illness, it can lead to brain and liver damage.

53
Q

What is the mechanism of action of aspirin?

A

Aspirin irreversibly inhibits Cyclooxygenase 1 (COX 1), blocking the production of prostaglandins and thromboxanes. It is an irreversible inhibitor of COX 1, while non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen are reversible inhibitors.

54
Q

What is the effect of aspirin on platelet function?

A

Aspirin decreases the production of thromboxane, which reduces its binding to the thromboxane receptor. This leads to decreased platelet adhesion, activation, and aggregation. However, high doses of aspirin can inhibit the production of both thromboxane and prostacyclin, which may counteract the desired inhibition of platelet aggregation.

55
Q

What are the main uses of aspirin?

A

Aspirin is commonly used in patients with established vascular diseases such as ischemic heart disease (myocardial infarction, angina), cerebrovascular disease, and peripheral vascular disease. It improves prognosis, reduces mortality, and decreases adverse events like heart attacks and strokes.

56
Q

What is the significance of aspirin as a drug?

A

Aspirin is considered a mainstay drug due to its affordability and effectiveness in preventing and managing various cardiovascular conditions.

57
Q

What is the mechanism of action of Clopidogrel?

A

Clopidogrel is a platelet P2Y12 receptor inhibitor. It blocks the binding of ADP to the P2Y12 receptor on platelets, thereby reducing platelet aggregation, activation, and adhesion.

58
Q

What is the use of Clopidogrel?

A

Clopidogrel is used as part of dual antiplatelet therapy (DAPT) following a myocardial infarction (MI) or elective coronary stenting. It is also used as a first-line treatment for peripheral arterial disease and in patients with recurrent stroke despite aspirin therapy.

59
Q

What are the side effects of Clopidogrel?

A

The main side effects of Clopidogrel include bleeding, which can affect the timing of major surgeries, and rash. It is important to note that up to 30% of individuals may not achieve the full effect of the drug, leading to potential Clopidogrel resistance.

60
Q

What is the role of Glycoprotein IIb/IIIa receptor inhibitors, such as Tirofiban?

A

Glycoprotein IIb/IIIa receptor inhibitors act on the final common pathway of platelet aggregation. These drugs are highly potent anti-thrombotic agents but carry a high risk of bleeding. They are typically given during high-risk coronary stent procedures and primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) and high-risk coronary anatomy.

61
Q

What is the mechanism of action of Warfarin?

A

Warfarin inhibits the production, specifically gamma carboxylation, of vitamin K-dependent coagulation factors 2, 7, 9, and 10. It also inhibits the production of natural anticoagulants protein C and S.

62
Q

What are the clinical uses of Warfarin?

A

Warfarin is the drug of choice for patients with mechanical heart valves and mitral stenosis with atrial fibrillation. However, it is being superseded by direct oral anticoagulants (DOACs) for stroke prophylaxis in atrial fibrillation, treatment of deep vein thrombosis (DVT), and pulmonary embolism (PE).

63
Q

What are the main side effects of Warfarin?

A

The main side effect of Warfarin is bleeding, which can be managed with slow reversal using vitamin K or rapid reversal using blood factors like prothrombin complex concentrate or fresh frozen plasma. Warfarin is also known to be teratogenic, crossing the placenta and posing a significant concern, particularly in the first trimester. Other side effects include warfarin-induced skin necrosis and a transient hypercoagulable state during warfarin induction, requiring overlap with heparin.

64
Q

What is the mechanism of action of Heparin?

A

Heparin enhances the effect of the natural anticoagulant antithrombin (AT). It binds to AT and activates it, leading to the inhibition of coagulation factors 2, 7, 9, 10, 11, and 12.

65
Q

How is the therapeutic effect of Heparin measured?

A

The therapeutic effect of Heparin can be measured by monitoring the activated partial thromboplastin time (APTT), which reflects the activity of the intrinsic pathway. The goal is to achieve an APTT that is 1.5-2.5 times the control value.

66
Q

What are the side effects of Heparin?

A

The main side effect of Heparin is bleeding. The antidote for Heparin overdose is protamine, which acts as a potent vasodilator.

67
Q

What is the role of unfractionated Heparin?

A

Unfractionated Heparin is still used in specific situations such as chronic kidney disease, dialysis, and bypass machines where its use is warranted.

68
Q

What are low molecular weight heparins (LMWHs)?

A

Low molecular weight heparins, such as Enoxaparin and Tinzaparin, are given subcutaneously and have reliable absorption. They do not require monitoring. These drugs are used acutely for conditions such as myocardial infarction (MI), atrial fibrillation (AF), pulmonary embolism (PE), iliofemoral deep vein thrombosis (DVT), and for venous thromboembolism (VTE) prophylaxis.

69
Q

What is Heparin-induced thrombocytopenia (HIT)?

A

Heparin-induced thrombocytopenia is a potentially dangerous side effect of heparin therapy. It is more common with unfractionated heparin (UFH) than with low molecular weight heparins (LMWH). HIT is caused by antibodies that bind to complexes of heparin and platelet factor 4 (PF4), leading to platelet activation and a prothrombotic state. It is characterized by a falling platelet count and can result in the extension of a previously diagnosed blood clot or the formation of new blood clots elsewhere, including skin necrosis.

70
Q

What are DOACs?

A

DOACs (Direct Oral Anticoagulants) are a class of anticoagulant medications. Examples include Rivaroxaban and Apixaban, which are factor Xa inhibitors, and Dabigatran, which is a direct thrombin inhibitor.

71
Q

What are the main uses and advantages of DOACs?

A

DOACs are used for various indications such as treating deep vein thrombosis (DVT), pulmonary embolism (PE), and atrial fibrillation (AF). They are also used for post-hip/knee replacement prophylaxis. DOACs offer more reliable anticoagulant action than warfarin. Higher doses provide greater effectiveness with similar bleeding risks, while lower doses maintain efficacy while reducing the risk of bleeding. DOACs also have fewer drug interactions compared to warfarin. Dabigatran has an antidote called Idarucizumab, while Rivaroxaban and Apixaban have an antidote called Andexanet.

72
Q

What are the main treatments for haemophilia?

A

The main treatments for haemophilia involve the use of recombinant factor VIII or factor IX infusions. These infusions aim to raise the levels of the deficient clotting factor to 50-100% of normal. Prophylactic infusions are administered every 2-3 days, while on-demand infusions are given when bleeding or injury occurs. Gene therapy, using a modified virus to introduce a copy of the gene that encodes for the missing clotting factor, is also being explored as a treatment option.

73
Q

What are the main treatments for von Willebrand disease (vWD)?

A

The treatment options for vWD include the use of desmopressin (DDAVP), which increases the synthesis and release of von Willebrand factor (vWF) and factor VIII. Anti-fibrinolytics, such as tranexamic acid, can be used to reduce thrombus breakdown. Plasma products can also be administered to replace vWF and factor VIII.

74
Q

How is vitamin K used in the treatment of bleeding disorders?

A

Vitamin K is used to treat vitamin K deficiency and to reverse the effects of warfarin, an anticoagulant medication. Vitamin K is administered in cases of fat malabsorption, biliary obstruction, haemorrhagic disease of the newborn (given 1mg at birth), and in patients receiving warfarin treatment. Vitamin K is essential for the gamma carboxylation of vitamin K-dependent factors, including factors X, IX, VII, II, as well as proteins S and C.

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